VOLUME 6 - NUMBER 2 - 2026

Menopause and reproductive endocrine dysfunction in CKD-associated osteoporosis

  • Sukanya Sakthivel, Maria Fusaro, Althea Cossettini, Hanne Skou Jørgensen
  • Concise reviews, 73-78
  • Full text PDF

  • Chronic kidney disease (CKD) is associated with multiple comorbidities and adverse outcomes, including cardiovascular disease and skeletal fragility. Women with CKD exhibit increased fracture risk, exacerbated by traditional osteoporosis risk factors and CKD-related alterations in mineral and endocrine regulation. Reproductive endocrine dysfunction, including hypogonadism, amenorrhea, and early menopause, is common in CKD. Mechanisms include accelerated uremia-related follicular atresia, hypothalamic–pituitary–ovarian axis disruption, and elevated prolactin, endorphins, and leptin. Amenorrhea may be misclassified as menopause, complicating risk assessment. These alterations contribute to impaired bone remodeling and increased cardiovascular risk, with early menopause linked to higher mortality. Kidney transplantation may restore hypothalamic–pituitary–gonadal function and fertility, pointing to a reversible component of CKD-associated hypogonadism. Hormone replacement therapy or selective estrogen receptor modulators may improve bone density and reduce fracture risk, although evidence remains limited. Long-term safety is not established in the setting of kidney dysfunction, and caution is required when prescribing these therapies to patients with CKD. Overall, reproductive aging and endocrine dysfunction in women with CKD remain under-recognized and warrant further investigation.

  • KEY WORDS: Chronic kidney disease, fracture, hormone replacement therapy, hypogonadism, osteoporosis, sex hormones.